Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Endocrine > Peters Lectures > Flashcards

Peters Lectures Flashcards

1
Q

How is specificty of signalling achieved in the endocrine system?

A
  • chemically distinct hormones
  • specific receptors for each hormone
  • distinct distribution of receptors across target cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the difference between the glands in the endocrine and exocrine systems?

A

endocrine glands are ductless

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the 4 chemical types of homrone?

A

modified amino acids; steroids; peptides; proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the features of hormone control?

A

act a low concentration over large distances to activate specific receptors with high potency to integrate organ function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How is hormone action terminated?

A

by enzyme-mediated metabolic inactivation in the liver or at sites of action

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How are amine hormones stored and released?

A

pre-synthesised, stored in vesicles. when ligand binds to cell receptor, calcium enters the cell and mediates exocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How are peptide and protein hormones stored and released?

A

pre-synthesised usually from a longer precursor, stored in vesicles, released in response to stimuli by calcium-deoendent exocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What enzymes convert the precursor protein to the mature hormone?

A

convertases during intracellular transport

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the difference between steroid synthesis and release compared to that of amines and proteins?

A

steroids are synthesised and secreted upon demand, are not presynthesised and stored in vesicles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What effect does stimuli have on the synthesis of steroids?

A

stimuli increase:

  • cellular uptake and availability of cholesterol
  • rate of conversion of cholesterol to pregnenolone (rate limiting step)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the functions of carrier proteins?

A

to increase amount of hormone tranported in the blood; provise a reservoir of hormone and extend the half-life of the hormone in the circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are two important general carrier proteins?

A

albumin; transthyretin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Why does free concentration of hormone not rise abruptly?

A

surges in hormone secretion are buffered by biding to carriers-they mop up the extra hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What type of hormone can corss the capillary wall to activate receptors in target tissues?

A

free hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the main determinant of plasma concentration?

A

rate of secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What factors contraol secretion?

A

negative feedback; neuroendocrine (eg stress); diurnal rhythm (rate fluctuates as a function of time)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What does tropic mean in relation to hormones?

A

a hromone that acts upon a nother endocrine gland to resulgate its secretion of hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Aside from secretion, what other factor contributes to plasma concentration?

A

rate of elimination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the 3 types of hormone receptor?

A

GPCR; receptor kinases; nuclear receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the classes of nuclear receptor?

A

class 1; class 2 and hybrid class

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What hormone activates class 1?

A

steroid hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What do class 1 recetpros do in absence and presence of activating ligand?

A

in absence- located in the cytoplasm bound to inhibitor heat shock proteins, when activated, move to the nucleus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What type of hormone activates class 2 nuclear receptors?

A

lipids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Where are class 2 receptors found?

A

in the nucleus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What hormones act of hybrid class of receptors?

A

thyroid hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What other class of receptor is hybrid class similar to?

A

class 1

27
Q

What enzyme converts ATP to cAMP?

A

adenylyl cyclase

28
Q

What does cAMP do?

A

increases the amoutn of protein kinase A which phosphorylates target proteins

29
Q

What type of G protein increases action of adenylyl cyclase?

A

Gs

30
Q

What type of G protein inhibits adenylyl cyclase?

A

Gi

31
Q

What enxyme does Gq receptors increase the activity of?

A

phospholipase C

32
Q

What two molecules does phosphlipase C create from PIP2?

A

IP3 and DAG

33
Q

What is the action of DAG?

A

activates protein kinase C which phosphorylates target proteins

34
Q

What does IP3 do?

A

works on IP3 receptors on the endoplasmic reticulum(or sarcoplasmic reticulum in muscle cells) to `release calcium

35
Q

Give an exmple of a hormone which signals via receptor kinases?

A

insulin

36
Q

What does binding of a ligand to a receptor kinase cause?

A

autophosphorylation of intracellular tyrosine residues

37
Q

What proteins do the phosphorylated tyrosines then phosphorylate?

A

insulin receptor substrate proteins

38
Q

What happens to the class 1 nuclear recetor when it moves into the nucleus (when activated and bound to steroid)?

A

forms a dimer and binds to hormone response elements in DNA

39
Q

What does the binding of the dimer to hormone receptor elements inthe DNA cause?

A

transcrition of specific genes to tbe switched on (transactivated) or switched off (transrepressed)

40
Q

What are the 4 methods of action of drugs for T2DM?

A

increasing secretion of insulin; decreasing insulin resistane and reducing hepatic glucose output; slowing glucose absorption from the GI tract; enhancing glucose excretion by the kidney

41
Q

What drugs at by increasing secretion of insulin?

A

SUs; incretin mimicsl glinides; gliptins

42
Q

What causes the Katp channel to open?

A

ADP-Mg binding to the SUR1 subunit

43
Q

Give examples of sulfonyureas?

A

tolbutamide; glibenclamide; glipizide

44
Q

What is the action of SUs?

A

displace the binding of ADP-Mg from the SUR1 subunit

45
Q

What are the side effects of SUs?

A

hypoglyaemia; weight gain

46
Q

How do glinides work?

A

bind to SUR1 to close the Katp channel

47
Q

Why are glinides less likely to cause hypoglycaemia than SUs?

A

have rapid osnet/offset kinetics

48
Q

What are the actions of GLP-1?

A

enhance insulin release; delay gastric emptying; decrease glucagon release

49
Q

Give an example of an incretin analogue?

A

extenatide

50
Q

How does extenatide work?

A

binds to GPCR GLP-1 receptors that increase intracellular cAMP conc.

51
Q

What are actions of extenatide?

A

increases insulin secretion; suppresses glucagon secetion; slows gastric emptying and decreases appetite

52
Q

How is extenatide administered?

A

subcutaneously

53
Q

What are the side effects of extenatide?

A

nausea; hypo; pancreatitis

54
Q

What does the enzyme dipeptidyl peptidase-4 do?

A

temrinates the actions of GLP-1 and GIP

55
Q

What is the mode of action of gliptins?

A

competitively inhibit DPP-4, prolonging the actions of GLP-1 and GIP

56
Q

What is alpha-glucosidase?

A

a brush border enzyme that breaks down starch and disaccharides to absorbale glucose

57
Q

What are the side effects of alpha-glucosidase inhibitors?

A

flatulence; loose stools; diarrhoea; abdominal pain; bloating

58
Q

What are the actions of metformin?

A

reduces hepatic gluconeogensis; increases glucose uptake; reduces carbohydrate absorption; increases fatty acid oxidation

59
Q

What are the good things about metformin?

A

doesnt cause hypos; causes weight loss

60
Q

What are the side effects of metformin?

A

GI upset; lactic acidosis

61
Q

What is the mode of action of TZDs?

A

enhance the action of insulin at target tissues by acting on the PPARy nuclear receptor

62
Q

What are benefits of TZDs?

A

promote FA uptake and storage in adipocytes rather than in SK and liver; reduces hetpatic glucose output

63
Q

What are the adverse effects of TZDs?

A

weight gain; fluid retention; increased incidence of bone fractures

64
Q

What is the action of SGLT inhibitors?

A

act to selectively block the reabsorption of glucose by SGLT2 in the proximal tubule of the kidney tubule

Endocrine (27 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions